Uts vol4

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publication

Undergraduate Research Magazine With Proceedings of the Biological Sciences Student Research Showcase 2013

Up close and personal

This photo was taken of a single leaf using purely sunlight as the backlight. The light allows a clear representation of the veins and Under the Scope the amazing networks are formed.

Division of Biological Sciences University of California, San Diego sqonline.ucsd.edu sq.ucsd.edu

Volume 4 2013-2014

Division of Biological Sciences

Just as the field of science continues to evolve and grow over time, so does Saltman Quarterly.

This year, the Saltman Quarterly program expanded its reach by publishing weekly online articles on topics ranging from student profiles to current biological happenings at UC San Diego to recent research findings as well as student-life blogs on sqonline.ucsd.edu. In addition, we began printing quarterly newsletters featuring some of these online articles to bring the news directly to our fellow students. Our talented group of writers not only worked hard to create intriguing articles for SQ Online, but also worked together to present student research from UC San Diego’s annual Biological Sciences Student Research Showcase in the publication you are now holding in your hands: Under the Scope.

For the fourth year in a row, Under the Scope will showcase research done by undergraduate students here at UC San Diego in such a manner as to communicate science to biologists and non-biologists alike. Staying true to our inspiration, Dr. Paul Saltman, we aim to make science accessible and spread a passion for science that can touch

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broad groups of people. What truly makes this publication special is the student voice that is present in the research, writing, art, and design of Under the Scope.

This year’s issue of Under the Scope was brought to life by the creativity of both teams of student authors and artists who collaborated to share the cutting-edge scientific discoveries presented at the Student Research Showcase. Each piece in the publication represents a junction between exciting scientific happenings and the implications of these discoveries in our everyday lives.

Along with my fellow editors, I am delighted to present to you the fourth volume of Under the Scope. This volume will take you on a journey that highlights various topics that were presented at the 2013 Biological Sciences Student Research Showcase ranging from the connection between breastfeeding and HIV to a drug discovery for treating malaria, just to name a couple. Read on to be inspired by the amazing innovations and developments happening at our university.

Editorial Board

Staff Advisors

Faculty Advisory Board

Writers

Illustrators

Executive Editor Sameeha Khalid

Associate Dean for Education Gabriele Wienhausen, Ph.D.

Features Editor Mandeep Bajwa

Manager, do/bio Center Hermila Torres

Cellular and Developmental Biology Emily Troemel, Ph.D. Steven Wasserman, Ph.D.

Production Editor Michaela Go

Ackowledgements

Ecology, Behavior and Evolution Heather Henter, Ph.D.

ACMS Web and Graphic Designer Elaine Fleming

Molecular Biology David Holway, Ph.D.

Justine Liang Elizabeth Cai Grace Park Bianca Chong Jamie Yoon Wenpei Li Aimee Ermel

Director of Science Communications, Division of Biological Sciences Kim McDonald

Neurobiology Kathleen French, Ph.D.

Maximo Prescott Edgar Villaruel John Nichols Alisha Jain Rubeena Basra Anna Nidhiry Maria Tran Safwan Haque Briana Kusuma Natalya Ballard Amanda Shelton Anna Alvarado Jennifer Park Christina Cui Amaris Garcia

Features Design Editor Dilara Onur

Sameeha Khalid Executive Editor, Under the Scope

Technical Editors Jasmine Chau Sveta Mohan

Director, Writing Center Madeleine Picciotto, Ph.D.

Cover Illustration

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PHENOMENON OF PAIN Written by Alisha Jain, Rubeena Basra, Anna Nidhiry

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DIMMED LIGHTS Written by Jennifer Park, Christina Cui, Amaris Garcia

HIV AND BREASTFEEDING

Written by Maria Tran, Safwan Haque, Briana Kusuma

THE GAMETOCYTE PROJECT Written by Maximo Prescott, Edgar Villaruel, John Nichols

15 Illustration by Aimee Ermel Based on illustration from The National Encyclopedia

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LEIGH’S SYNDROME Written by Natalya Ballard, Amanda Shelton, Anna Alvarado

BIOLOGICAL SCIENCES STUDENT RESEARCH SHOWCASE 2013

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Dimmed Lights

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very Christmas, homes across the nation cocoon themselves in swathes of flickering lights. The flashing signs and dazzling scenes are absolutely mesmerizing—even if there happens to be one or two tiny burnt out bulbs, no one would notice. If strings of empty lights were to accumulate, however, the passerbys might begin to notice that something is off.

Now, what if each light was a neuron? Every bulb that blinks out is a brain cell leaving gaps in crucial chains of communication and production. From losing important compounds to accumulating dangerous by-products, the effect would become more and more apparent as larger proportions of neurons faded away. Like any set of Christmas decorations, whole sections of the scene would eventually be crippled. If this phenomenon were to occur in a particular region of the brain known as the substantia nigra, the major loss would be concentrated in our motor functions, leading to the disease known as Parkinson’s disease.

Such a scenario has already impacted the lives of around one million Americans. Symptoms manifest with slight tremors, barely noticeable in the overall quality of life until further progression occurs. Impairment of overall movement leads to difficulty in walking, which escalates to potential mental effects—the symptoms only continue to snowball. But these primary symptoms, known as bradykinesia and Parkinson’s gait, may take years to develop in some patients, time that exponentially

Illustration by Elizabeth Cai

hinders the effectiveness of the treatment. If there was a method through which Parkinson’s disease could be easily identified, the lost time could be made up and countless cases improved.

Causes Before a solution to Parkinson’s disease can be considered, first the cause of Parkinson’s must be identified. Parkinson’s progresses as more and more neurons in the substantia nigra deteriorate. These neurons produce the vital chemical messenger dopamine, which allows communication between the substantia nigra and another area of the brain known as the corpus striatum which translates to the coordination of smooth and balanced muscle movement. Therefore, a lack of dopamine causes a loss in the ability to control body movements.

Why Parkinson’s disease occurs and how the neurons become impaired is not known. There is evidence that Parkinson’s disease may be genetically inherited; in a small number of families, specific genetic abnormalities leading to the illness have been identified. It is probable that cases of people who develop Parkinson’s disease early in life, called young-onset Parkinson’s disease, are influenced by a genetic component. However, the vast majority of people with Parkinson’s disease do not have one of these identified genetic abnormalities. Interestingly, there is also some evidence that certain toxins in the environment may cause Parkinson’s disease. Scientists have

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suggested that external or internal toxins may selectively destroy the dopaminergic neurons, causing Parkinson’s disease. Toxins that may be linked to Parkinson’s disease include manganese, carbon monoxide, carbon disulfide, and some other pesticides. Despite the uncertainty as to what causes Parkinson’s disease, treatments exist and research is relentlessly seeking a cure.

Symptoms The most notable symptom of Parkinson’s disease is abnormal movement. Typically, signs start to appear during ages 50 to 60. The earliest and most common sign is indicated by the rigidity and aching of muscles.

Then, slow and limited movement become noticeable.

For instance, lifting your body out of a chair or shifting in bed becomes increasingly difficult. Various parts of the body move differently and with more difficulty. As Parkinson’s disease gets worse, difficulty with walking and balance are felt. A person with Parkinson’s disease is likely to take small steps and shuffle with his or her feet close together, bend forward slightly at the waist, and have trouble turning around. Dr. Irene Litvan’s research centers around these abnormal movements.

Although tremor is one of the most common signs of Parkinson’s disease, not everyone with tremor has Parkinson’s disease. Unlike tremor caused by Parkinson’s disease, tremor caused by other conditions gets better when your arm or hand is not moving and gets worse

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when you try to move it. The most common cause of non-Parkinson’s tremor is essential tremor, a treatable condition that is often wrongly diagnosed as Parkinson’s disease. Incorrect diagnosis is extremely problematic. Dr. Litvan’s laboratory recognizes the need for an effective method to accurately identify the presence of Parkinson’s disease. Currently, her lab is developing a device to aid clinicians and correctly identify Parkinson’s Disease.

Research Dr. Litvan’s research uniquely combines the physical evaluation of Parkinson’s disease with modern day technology. Her research seeks a better understanding of neurodegenerative disorders that present Parkinson’s or dementia symptoms. In one facet of her research, her team has been trying to develop an effective diagnostic tool for neurological disorders like Parkinson’s disease for physicians to produce more accurate evaluations for patients. Using motion tracking algorithms and Microsoft Kinect, her team has been able to detect specific movements that are clinically relevant for indicating the presence and severity of Parkinson’s disease.

The primary goal for their research is the ability for the device to detect the severity of a disorder over time and, based on the evaluation from the device, accurately tailor drugs and treatment. Currently, physicians evaluate the presence of Parkinson’s disease and the patient’s severity by intuition: there is no actual medium to accurately

The figure above shows the progression of Parkinson’s disease. It starts at the substantia nigra (shown in red) and, as time progresses, different parts for the brain start to degrade or become diseased.

diagnose patients.

“Our scales are still subjective because it is hard to remember exactly how someone moves. Here we would have a device that we could exactly measure the movements of individual patients. We can translate this data into values which would be very helpful for clinicians in several applications like clinical trials,” said Dr. Litvan.

Having better and more accurate evaluations is imperative for proper patient care. Because several evaluations are inaccurate or non-specific, many therapies lack

clear benefits because the right instruments are not implemented to measure improvement. Compact and easy to use devices that measure speed and movement in physician offices create the opportunity for fewer unnecessary treatments and better results.

Dr. Litvan chose to use Microsoft Kinect for multiple reasons. The primary reason is the price point: most motion tracking systems range from 10 to 100 thousand dollars while Kinect averages around 100 dollars. Physicians are much more likely to adopt a cost efficient option in their offices and clinics.

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Kinect uses motion analysis to break down data. The “This is a dream project to be working on. The fun part movement of the patient is evaluated by a series of is working out how [Kinect] is clinically relevant,” said dots. These dots indicate each joint and ligament in the senior Neil Gandhi. human body. As the patient is instructed to do different commands such as walk to the end of the room and “Our Dr. Litvan and her lab’s sophisticated use of a simple turn around, the motion sensor analyzes the angle scales gaming system is indeed incredible. As more and displacement of each of the dots through a are still and more trials are conducted, a large body of subjective standardized data can be collected and, because series of basic algorithms. Undergraduates were because it is of the sheer volume, patterns not recognized responsible for writing the motion tracking hard to remember before can be identified. Patient coordinates algorithms for movements and delays that are exactly how someone can be compared against information from clinically relevant. moves. Here we would people around the world, allowing for have a device that we earlier and more precise diagnosis.

Still, there are many limitations to could exactly measure the This ability is crucial, since current using Kinect. Kinect is only able to movements of individual patients. diagnosis guidelines are subjective analyze movement in one dimension versus a three dimensional view. We can translate this data into values in nature and limit the ability of Current devices that detect three- whichwouldbeveryhelpfulforclinicians doctors without a movement dimensional movement are still in in several applications like clinical trials,” disorder specialization said Dr. Litvan . to accurately diagnosis the testing phase and extremely patients or pool data. The costly. Additionally, assessing standardized biomarker Parkinson’s disease by being developed in Dr. movement is only one Litvan’s lab, however, extends that ability to a larger method. The disease also manifests in neurological physician population, and, when coupled with the problems and digestion issues. Dr. Litvan’s team will algorithm’s ability to diagnose early symptoms, allows begin a pilot study with 10 to 20 people in the near a larger population of patients to be able to receive early future to evaluate the Kinect’s strengths and weaknesses. treatment. Early diagnosis will delay the need for strong “There is also potential for the device to distinguish medication such as Levodopa, which, although effective other disorders those above the age of 65, for instance, for symptomatic treatments, has very strong side effects. falling,” said Dr. Litvan The use of a low cost platform is another plus, since it

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allows for further implementation of the technology.

The algorithm also has a flexibility built within it that allows the computer coding to adapt to more elegant motion tracking systems as they become available. As mentioned, the main difficulty lies with balancing the cost of the motion tracking device with the precision of the technology: as the prices of these systems fall, the algorithm can be easily adapted to the greater power.

However, it isn’t just the motion tracking device that requires time to become suitable for medical use. Because Parkinson’s disease is manifested over a wide set of symptoms, a fully integrated perspective requires data from electroencephalography (EEG), eyetracking, and other forms of cognitive evaluations. By constructing algorithms and infrastructure for objective evaluations of these areas, a more holistic yet objective diagnosis of Parkinson’s disease may be reached.

Coupling all these advancements with developments in bioinformatics, physicians may one day have the power to compare patient data against the information collected from thousands of people across the world. The extensive volume of data that can be collected through these diagnosis advancements will provide insight into the nature of Parkinson’s disesase and, through a topdown analysis, researchers can begin to more accurately pinpoint where and how particular neurons are blinking out. By uncovering the very root of neuronal death in Parkinson’s disease, a whole range of treatment possibilities

may be opened. In fact, any neurological disorder that manifests in motion dysfunctions can be categorized by this algorithm, providing greater comparative data and insight into the human brain.

It may seem as if Parkinson’s disease is still largely shrouded in uncertainties, but through diagnosis breakthroughs such as Dr. Litvan’s lab, physicians are increasingly empowered to precisely pinpoint symptoms. As technology develops in motion tracking and adjunct fields, more and more standardized information may be collected regarding Parkinson’s disease. Perhaps one day we may hope to find a treatment effective enough to eliminate the stigma associated with having Parkinson’s disesase.

Perhaps one day, fixing a neuronal pathway will be as simple as fixing your Christmas lights.

WRITTEN BY JENNIFER PARK, CHRISTINA CUI, AND AMARIS GARCIA. Jennifer is a Public Health major. She will graduate in 2016. Christina is a Physiology and Neuroscience major. She will graduate in 2017. Amaris is a Physiology and Neuroscience major. She will graduate in 2016.

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HIV and Breastfeeding

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icture this: you’re living in an underdeveloped country on a budget of 20 dollars a month. You and your family often struggle to decide which necessities should be prioritized because your income is not enough to sustain you and your loved ones comfortably.

Add an infant to the mix and you have another mouth to feed. Normally, babies can be breastfed, but what happens when the mother is HIV positive?

This is a dilemma facing many mothers in third world countries who often struggle with deciding whether to starve their child or possibly infect them with HIV.

The Villain: HIV Human Immunodeficiency Virus (HIV), is best known as the precursor to Acquired Immunodeficiency Syndrome (AIDS) and affects around 33.4 million people worldwide, most of them in third world countries. Usually transmitted through unprotected sex, contaminated needles, breastfeeding, or being born to an HIV-positive mother, this virus suppresses the immune system of a patient by killing cells that are important to the immune response. Even with all the research that is taking place, no cure for HIV has been found yet.

Part of the difficulties in finding a cure can be contributed to the way that HIV invades the human body, which is the host. HIV virions are shaped like spheres with nail-like protrusions. Inside of this cell, there is another spherical “core” full of HIV’s genetic information, such as RNA.

Illustration by Grace Park

This HIV virion fuses with the host’s cell by combining its own membrane with the host’s. The core then opens up and HIV’s RNA combines with the genetic material within the host cell’s nucleus. Once HIV proteins are synthesized, they push out of the cell and enter others, spreading the virus. The primary types of cells impacted

by HIV are the T helper cells, CD4+ cells, or monocytes (engulfing cells) of the immune system. With the T helper cells unable to announce the presence of the virus, the rest of the immune response cannot be initiated. This means HIV can go undetected by the body, allowing the virus to lay dormant and replicate-all while the immune system grows weaker and leaves the host vulnerable to pathogens (germs that cause disease) that may prove fatal.

The New Sheriff in Town: HMOs Over the years, there has been research focusing on the prevention of HIV transmission between mother and child. Dr. Lars Bode’s lab at the UC San Diego School of Medicine has discovered that, contrary to the popular belief that breastfeeding leads to the infant receiving the HIV virus, breastfeeding may actually help prevent the spread of HIV-1 due to a component in breast milk called the Human milk oligosaccharide.

Human milk oligosaccharides (HMOs) are a family of carbohydrate molecules that can be found in human breast milk and have been strongly associated with the prevention of diseases and infections in newborn children.

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HMOs supposedly help protect human infants, but they also stop animals from feeling the pain of an immune response caused by inflammation. They interact with the body’s immune receptors, which bind to pathogens and signal for other immune cells to destroy it. Although there has been no actual proof that HMOs actively stop the spread or transmission of disease, it has been widely speculated by numerous researchers based on data from lab experiments.

The figure above shows HIV and HMO competing for the same binding site. Normally HIV binds to a receptor called a DCSIGN (Dendritic Cell-Specific ICAM3-Grabbing Non-integrin) which transfers the HIV to CD4+ T Lymphocytes. Once HIV binds to the CD4+ T lymphocytes or helper T cells it can begin its pathogenicity. HMOs prevent this from ever happening by binding to the DC-SIGN and preventing HIV from binding instead. Figure courtesy of Dr. Lars Bode.

Being the third most abundant molecule in breast milk, HMOs play an important role in the development of the infant gut. These molecules linger in the mucouslined surfaces of the gastric tract, where they act as food for beneficial bacteria that potentially ward off other infectious pathogens by taking the resources needed to grow. Another way that they protect the child from illness is by acting as epithelial cells (which make up the tissues of human bodies) and mimicking the receptors of actual epithelial cells so that the pathogens attach to HMOs instead of destroying the real cells. Not only do

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Dr. Lars Bode and His Experiment “There must be a reason why the oligosaccharides are there—the driving force being exposure to a lot of bacteria and viruses and parasites,” explained Dr. Bode, “In the past, when hygiene wasn’t that great, the infant really benefitted from those things [oligosaccharides] serving as decoy receptors or infectious agents.”

When it was found that only 10 to 15 percent of all breastfed infants were infected with HIV-1 without vaccines or therapies, Dr. Bode and his team of researchers, in collaboration with other laboratories, were curious about the inefficiency of breastmilk in transferring HIV1 from mother to offspring. They hypothesized that the presence of immunologically active factors in breast milk, such as HMOs, were responsible for this observation.

A specific concentration of HMOs, which was the median of the samples collected, was used as a standard

“Once we confirm of HIV transmission. It the protective was found that above nature of the certain this concentration HMO and understand of HMOs, infected mothers could not the protective transmit HIV to mechanism, we might their offspring. be able to translate the Although HMOs had the general trend information to other of preventing HIV types of transmission transmission, one HMO in particular [like sexually called 3’-SL had a transmitted HIV],” higher concentration in said Dr. Bode. HIV-transmitting mothers

than in non-transmitting ones. These HIV-transmitting mothers had greater HIV RNA load, a lesser number of immune cells, and higher amount of the virus in the body, all of which were associated with a higher degree of 3’-SL. HMOs, as represented by the research, can play on both teams - the team that hurts and the team that helps.

However, in terms of immune responses, they favor the helping team more. When infants do acquire HIV infection through breast milk, it is because the HMOs are not favoring the immune response or are simply inactive through mutation or absence, though it may also be due to the mother having the wrong type of HMO.

The Future of the Battle Against HIV The critical question remains: does the identity of the specific type and standard concentration of the HMO preventing HIV transmission have therapeutic value?

Answering this question may help scientists come up with curative drugs as opposed to antiretroviral drugs, which have to be maintained throughout one’s life to keep HIV inactive. Perhaps these drugs can eliminate transmission through breastmilk and also halt infection in adults. However, despite all these possibilities, there is still much to be learned before any direction in HIV prevention can be taken.

“Ideally, we would like to learn from nature and identify natural protection mechanisms and then use them in a broader context. At this point, we don’t really know [if and how] HMO reduces transmission. Once we confirm the protective nature of the certain HMO and understand the protective mechanism, we might be able to translate the information to other types of transmission [like sexually transmitted HIV],” Dr. Bode said, “Again, a long way to go.”

WRITTEN BY MARIA TRAN, SAFWAN HAQUE, AND BRIANA KUSUMA. Maria is a Microbiology major.

She will graduate in 2016. Safwan is a Microbiology major.

He will graduate in 2015. Briana is a Human Biology major and Law and Society minor. She will graduate in 2016.

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F

ighting a genetic disorder requires that the body remedy its own deficiencies. It is devastating then, when an infant loses the battle before it even has a fighting chance. When Christine Shimizu was suffering from a genetic disorder called Leigh’s syndrome, modern medicine couldn’t save her from the mitochondrial malfunctions in her body. Her disease was characterized by a lack of muscular control and breathing; the body was debilitated by the damage of cellular dysfunction.

Leigh’s syndrome is a disorder that affects children in early infancy, causing impaired motor, respiratory, and cognitive functions. The source of the children’s suffering stems from a genetic mutation that affects cellular mitochondria. Mitochondria play an integral role in providing the human body with enough energy to function and survive. The consequences of the genetic mutation manifest in malfunctioning mitochondria that cannot provide enough energy to the tissues in the body.

For areas that depend on energy the most, like brain tissue and muscle tissue, damage appears inescapable.

Leigh’s Syndrome

Mitochondrial Malfunction

Illustration by Bianca Chong

The mitochondria is the only cellular organelle in the body that has its own DNA, further complicating the genetic components of this disease. Researchers in the Mitochondrial and Metabolic Diseases Center at UC San Diego are at the forefront of mitochondrial research, focusing on the mechanisms of mitochondrial disorders like Leigh’s syndrome. Co-directors Dr. Richard Haas

and Dr. Robert Navaiaux and their teams have focused their efforts on uncovering the mysteries underlying Leigh’s syndrome and other mitochondrial diseases.

According to Mrs. Shimizu, creator of the Christini Fund in memory of Christine, “The Christini Fund goal was to support Dr. Naviaux and his research and spread the awareness on mitochondrial disease and the help that can be found at the Mitochondrial and Metabolic Disease Center at UC San Diego”. Mitochondrial based disorders like Leigh’s syndrome exhibit symptoms that mirror those displayed in common age-related diseases like Parkinson’s disease. While Leigh’s syndrome is a disease that primarily affects children, research on the disorder can shed new light on the role that cellular mitochondria plays during aging. Research on mitochondrial disorders and functions has the power to not only treat devastating genetic disorders, but it may also provide the key to solving one of the oldest puzzles: how to stop the negative signs of aging.

Energy and the Mitochondria Dr. Haas and Dr. Navaiux have determined that the majority of mitochondrial diseases, including Leigh’s syndrome, are due to genetic mutations in the mitochondrial DNA. Mitochondrial diseases impact the major metabolic functions in our body that provide much needed energy to do work. These diseases often cause deficiencies in

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Having a mitochondrial disease is essentially like using a smartphone without charging it the night before; you don’t have enough energy supply to get through the day. the production of adenosine triphosphate (ATP), the body’s cellular source of energy. Leigh’s syndrome for instance, is typically caused by the disruption of a protein complex known as cytochrome c oxidase (COX). This protein is the final step in the process of creating ATP in the mitochondria. Without a constant supply of ATP, changes in the homeostatic balance in the body would be difficult to recover from.

“The way that many children die with mitochondrial diseases is an association with an otherwise minor infectious disease and it can be as simple as a cold or an ear infection,” said Dr. Naviaux,“What happens is that they actually get better from the actual infection, but about five to ten days after the infection is getting better they don’t have sufficient energy resources to repair the damage.” Having a mitochondrial disease is essentially like using a smartphone without charging it the night before; you don’t have enough energy supply to get through the day. Without sufficient energy, our body cannot heal properly.

Finding signs of mitochondrial disease is not as easy as searching for tell-tale symptoms, like one would when looking to diagnose other diseases like the flu; mitochondrial deficiencies could be the root of many diseases and therefore could show symptoms found in other diseases. Dr. Naviaux

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and other clinicians have been struggling with this fact.

Dr. Naviaux said, “The problem that confounds clinicians is that mitochondrial disease can affect any organ, produce any symptom at any age. So there are many, many facets that make it hard for people to grab onto.”

This fact makes the diagnosis of these diseases much more difficult since there are hundreds of genetic mutations that could possibly give rise to these disorders and these disorders are difficult to pinpoint. Therefore, focus is shifted towards identifying biochemical markers of mitochondrial diseases in order to evaluate the disorder in a fast and efficient manner.

Mitochondrial Research In order to understand the intricacies of mitochondrial function, Dr. Naviaux and his team delved into the very core of the mitochondria: its own DNA. Undergraduate researchers from UC San Diego are at the forefront of Dr. Naviaux’s work and are able to unravel the mysteries behind this unique mitochondrial identity. One such researcher was Kacie Paik, a recent graduate from UC San Diego who spent years working at the Naviaux lab.

She started as a student lab assistant and eventually became involved in the Dr. Naviaux’s research. One

The figure above shows just some of the disease conditions caused by mitochondrial dysfunction. Mitochondria are responsible for creating most of the energy needed by the body. When they fail, energy is hard to come by. If failure occurs throughout the body’s cells, whole systems begin to fail and the person’s life is severely compromised. These mitochondrial diseases primarily affect children, but adult onset is becoming more common. Figure by Wenpei Li.

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of her key projects involved analyzing and developing a method to count the exact mitochondrial DNA copy number (mtDNA CN) which help elucidate the impact of mtDNA defects on mitochondrial diseases. These copy numbers could be used as indicators for mitochondrial disease, increasing the efficiency of its discovery and identification.

“Any deviation from normal mtDNA Copy Number can be a signal of diseased states in patients,” said Kacie, “By developing mtDNA CN method, our lab was able to use [it] as a screening process, testing the severity of diseases, and as a tool to understand complex mechanisms of mitochondria’s role in disease pathways.”

Kacie’s work went above and beyond quantifying signs of mitochondrial diseases. She was able to apply her research in uncovering the link between mitochondrial changes and aging. She mastered real-time quantitative polymerase chain reaction (qRT-PCR), a research technique that simultaneously involves amplifying target DNA and quantifying it. This is like hitting the jackpot on the slot machine, with thousands of coins flying at you while at the same time sorting these coins into quarters, dimes and pennies.

“I isolated DNA of mice in various ages and studied their mtDNA copy number changes by real-time quantitative PCR method. Through this project, I learned about [the]

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aging process at the molecular level and how deeply involved mitochondria are in this process,” said Kacie.

The possibility of a mitochondrial disease should never be ruled out.

Kacie’s contributions to the lab help paint a clearer picture on what to look for in diagnosing mitochondrial diseases. The mtDNA and the analysis of its components and mutations is central to uncovering the qualities of these elusive mitochondrial diseases. According to Dr. Imo Scheffler, a UC San Diego faculty member known for his extensive knowledge regarding the mitochondria, the number of mutations in mtDNA are main indicators for the expression of symptoms.

Because of research being done in Dr. Naviaux’s lab we now have the ability to understand some of the basics surrounding mitochondria. Contributors including Kacie and also both past and current undergraduate researchers are helping to evolve our understanding even more.

“If [someone’s] fraction [of mitochondrial DNA] mutations are low then [they] may not have any symptoms but if that fraction gets to be 50 percent or 80 percent then the symptoms may start to appear,” said Dr. Scheffler, “The ratio [of mitochondrial DNA point mutations] determines if the symptoms of the disease are even there or noticeable.”

It is important to recognize that our body heavily relies on the mitochondria to work as efficiently as possible.

Kacie states, “Mitochondria are essentially involved in many diseases that we commonly see—diabetes, autism, blindness and obesity—but also involved in rare diseases, such as Leigh’s syndrome and Lesche-Nahyn disease.”

Therefore, mitochondria should never be overlooked when it comes to identifying and treating these diseases.

Future Directions Kacie was named the 2009 Christini Fund Undergraduate Scholar of the year. The UC San Diego Christini Fund is a current ongoing fund that Debbie Shimizu created in 1999 in memory of her daughter, Christine Shimizu.

Through the support of this fund multiple discoveries have been made. These discoveries include (but are not limited to) the discovery of the cause of Alpers Syndrome, the discovery of how the mitochondrion controls mammal wound healing in regards to tissue regeneration, the discovery of “oxidation shielding” in relation to the free radical signaling involved in diabetes and cancer, and discovery of a new class of medicines that have the possibility of leading to completely new treatment options for individuals with autism or other neurological disorders.

In order to advance the medical field and treatment options available to those who need them it’s extremely

vital that scientists understand the most basic components of all mammalian life; mitochondria and its relation to providing energy to enrich our own motor, respiratory, and cognitive functioning. More research focused on mitochondria has the potential to help many lives worldwide; from individuals with learning disorders, heart disease, thyroid dysfunctions, visual problems, and even the individuals affected from a mitochondrial disorder itself. With a deeper understanding of the mitochondria eventually scientists will be able to do amazing things in multiple biological fields from anti-aging treatment to slowing or speeding up body metabolisms to saving and treating victims of the mitochondrial syndromes.

To support mitochondrial research or learn more about the UC San Diego Christini Fund, go to: www.christini.org

WRITTEN BY NATALYA BALLARD, AMANDA SHELTON, AND ANNA ALVARADO. Natalya is a Biochemistry and Cell Biology major. She will graduate in 2016. Amanda is a Physiology and Neuroscience major and Psychology minor. She will graduate in 2017. Anna is a Human Biology major and a Political Science minor. She will graduate in 2015.

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Phenomenon of Pain

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ver experienced that tingling sensation of “pins and needles� in your hands? That uncomfortable feeling you get from sitting rigidly during a dull lecture or after a long plane ride, like your hands are being attacked by a thousand fire ants at once. Usually shaking it out, or some swift muscle movement will grant a quick recovery, but imagine having that constant nagging sensation of numbness permanently. This reaction, coupled with weakness, or a burning sensation, are typical symptoms of a condition known as chronic neuropathic pain. Nearly 20 million people in the U.S. suffer from neuropathy, and over 50 percent of diabetes patients suffer from peripheral neuropathy as well, according to the United States Centers for Disease Control and Prevention. A doctor may tell their patient that there is no current solution or treatment, leaving them frustrated.

In the field of science, nerve injury is a subject with few answers, and medications for pain relief are largely temporary. The subject of pain is somewhat of a black hole, with no permanent solutions or treatments. But if we delve into the molecular level of pain, scientists can study mechanisms that may grant clarity to the conundrum and potentially bring a lasting solution.

The human nervous system is split into two: the central nervous system (CNS) and the peripheral nervous system (PNS). While the central nervous system consists of the the brain and spinal cord, the PNS deals with nerves in the rest of the body. Think of it as a series of complex, interlacing highways sending electrical messages to and

Illustration by Justine Liang

from a main factory (your brain). Peripheral nerve injury, or peripheral neuropathy occurs when nerve axons in the PNS are damaged. This is a major issue since axons, threadlike structures that extend out of a neuron, conduct the electrical impulses that send messages throughout the PNS and to the CNS. The damage of these nerve fibers impair the transmission of these messages and send wrong signals to other parts of the brain resulting in the chronic state of neuropathic pain.

Unfortunately, at present there is no cure to chronic neuropathic pain. However, the Campana, Yaksh, and Shubayev labs at UC San Diego Department of Anesthesiology are currently taking strides to answering the neuropathic conundrum puzzling many doctors.

Sensitivity to Stimuli Say you are a diabetes patient trying to take a hot shower, but find it painful. Neuropathic pain could cause an increased sensitivity to temperature that can be difficult to ignore.

The Yaksh Lab is conducting ongoing research about neuroinflammation processes, lipid mediators (produced in response to extracellular stimuli), pharmaceuticals, and preclinical spinal toxicology. His lab is interested in the mechanisms and changes in the peripheral nervous system that cause individuals to experience pain as well as knowing the pathways and pharmacology of those systems. Essentially, a large focus of the lab is how neuropathy can derive from different factors such

as allodynia and hyperalgesia (pain from a normally non-painful stimulus or increased sensitivity to pain).

As Dr. Yaksh said, “We aim to understand how these chemotherapeutic drugs used in cancer therapy drugs alter the systems to mediate hyperalgesia—that is to say making non-painful stimuli painful.”

The Significance of Schwann Cells Dr. Shubayev’s research focuses on the different processes of neuronal injury and the variety of therapeutics for neurodegenerative disorders and pain. eus Medical Med N u cl ia,

Inc .

Dr. Shubayev said, “We are studying changes in sensory and motor systems, the specific dynamics of molecular Neuron with Neuron with myelin sheath myelin sheath interactions, using damaged experimental systems that model human conditions of painful neuropathy.” Dr. Shubayev and her colleagues are approaching neuropathy by studying the breakdown of proteins, myelin damage and repair, the inflammation of nerves and other parts of the nervous system as a mechanism of neuropathic pain and disorders.

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“I had the opportunity to focus on Schwann cell cultures and the effects of inhibitors such as TIMP-1 and MMP-9 and how these two factors interacted with one another and their effects on pain,” said Amy Nyguyen, a previous undergraduate researcher in Dr. Shubayev’s lab.

Studies on gene-targeted animals indicate that Schwann cell composition can cause sensory alterations that influence neuropathic pain. Schwann cells are support cells that wrap around nerve axons in the PNS to form the myelin sheath (an insulating layer that wraps around axons). They fundamentally assist in the quick and effective transmission of electrical impulses across the nerve axon through insulation and regeneration.

During neuropathic pain, these “support cells” cannot increase the speed of electrical conduction and their impairment prevents axon regrowth, resulting in permanent neuronal damage.

Therapeutic Tactics When an injury occurs within the peripheral nervous system, Schwann cells are responsible for regulating the several processes for cell recovery. Studies on genetically engineered mice showed how the mechanisms of the LRP-1 protein influence neuropathic pain. The presence of this protein promotes cell regeneration and sustainable interactions between Schwann cells and other parts of the peripheral nervous system including neurons and axons. The absence of this protein, as seen in the

Pain is the most common reason people seek medical attention,” said Dr. Shubayev studies, fosters deterioration of Schwann cell migration and transmission in response to peripheral injury. Dr. Campana and other researchers are on the quest to find a drug that can serve the same function as the LRP-1 protein in eliminating or reducing neuropathic pain.

The migration of Schwann cells during injury is essential in understanding the different states of neuropathic pain. Therapeutic techniques that prevent Schwann cell degeneration may be effective in counteracting the progression of painful peripheral neuropathies.

Other Causes of Neuropathy Irregular Schwann cell migration is not the only cause of neuropathic pain; there are other various contributing factors that can also cause neuropathy. Diabetes, chronic use of alcohol, and chemotherapy can damage nerves and cause neuropathy. These cause what are called microneuropathies that begin in a human’s hands or feet and cause tingling and numbing. Micro-neuropathies also cause sensitivity to touch and decreased tolerance of pain. These factors can contribute to peripheral nerve injury and influence neuropathic pain.

Future Implications “Pain is the most common reason people seek medical attention,” said Dr. Shubayev. Conducting research

on Schwann cells, immune response, myelination of the nerves, and pharmaceuticals can help researchers gain a better understanding about the mechanisms that can eliminate or reduce neuropathic pain. Dr. Yaksh said, “So the work that people like Dr. Calcutt, Dr. Campana, or Dr. Shubayev, and others in this area do is try to understand how these changes in the peripheral sensory axon and terminals, affect sensory processing and lead to these anomalous pain states.”

“I believe the field of pain research has an expansive future because of how much more can be discovered about pain,” said Amy Nguyen. A cure for pain would be a significant milestone affecting millions of lives.

Most importantly, it would improve the quality of life for many individuals. Marc Marino, a student who worked with Dr. Yaksh, said, “I don’t think anyone is going to find a magic bullet type drug for neuropathy, but as we progress in our understanding of the basic cellular and molecular mechanisms of these pain states we will hopefully find targets for small molecules to reduce or eliminate pain.”

WRITTEN BY ALISHA JAIN, RUBEENA BASRA, AND ANNA NIDHIRY. Alisha is a Human Biology major. She will graduate in 2016. Rubeena is a General Biology and Human Development double major. She will graduate in 2015. Anna is a Human Biology major. She will graduate in 2016.

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The Gametocyte Project:

A New Solution to a Global Problem

T

hey come for you in the night: winged, toothless, and hungry for blood. From still, septic waters they emerge, born of the wretched and vile parts of this Earth; the scourge of Man. In swarms they descend upon you, their hapless sleeping victim, and feast upon that vital fluid which courses through your veins. And then they are gone, vanished like a chanced specter, into the darkness from whence they came. You awake the next morning bearing the mark, an ill-fated omen foretelling the last of your days, chiseled into the flesh of your neck. Unbeknownst to you, you were visited the night before by one of the most dangerous and prevalent vectors of human disease: the mosquito.

Malaria: A Global Problem Malaria is a global health issue, with not only severe bio-medical consequences, but economic and social as well. In fact, it is a leading cause of death and disease in many developing countries, where pregnant women and young children are the groups most affected. According to the World Health Organization’s World Malaria Report, half the world’s population (3.3 billion people) live in areas at risk of malaria transmission in 106 countries and territories. In addition, malaria caused an estimated 216 million clinical episodes, and 655,000 of those led to deaths in 2010. On top of that, 86 percent of those deaths were children, the group most at risk for the disease.

As mentioned, malaria also has profound social and

Illustration by Jamie Yoon

economic effects, imposing substantial costs. Those infected with malaria are no longer able to work or they miss school causing either a loss in income or lack of education. Also, families of victims must devote their budget to malaria treatment, which in many cases is a substantial portion of their shared income leaving little money left over for necessities such as food and water.

Additionally, government costs include maintenance of health facilities, purchase of drugs and supplies, lost opportunities for joint economic ventures and tourism, and public health interventions against malaria, such as insecticide spraying or distribution of insecticide-treated bed nets. Direct costs in relation to illness, treatment, and premature death have been estimated to be at least 12 billion dollars per year. The current slow pace of drug discovery, drug development and clinical trials only add to the problems.

The Gametocyte Project Dr. Elizabeth Winzeler, from the Department of Pediatrics of the UC San Diego School of Medicine, leads a lab tackling this devastating global burden. While the genome for Plasmodium falciparum —the parasite responsible for causing malaria— has been sequenced, the exact functions of the genes within the genome remains unclear.

This gap in knowledge limits researchers from knowing what genes could be the best targets for new antimalarial drugs. Thus, the Winzeler Lab’s Gametocyte Project focuses on identifying the functions of genes within the

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“By ing block sformation s into of e n n t i a o r i s t s a r is the ia pa e transm major from Revelle College, “Results sometimes squito r o a l m a m s h o t t t n f t , e o even appear to be dependent on the phases cytes uman hos thus prev o t a e c m c of the moon.” ga Rebe rom h ted, and f d a i i r a mala is preven ction,” s When asked about his reason of joining fe r n i o t c f o this particular lab, Alan said, “I love the general ve ses a c basis of genetics because I believe it is the foundation new . malaria e p of life. This lab is perfect because it has a genetics based o parasite’s Stanh genome, so treatments can be developed specific to the most vital genes of the parasite.

The Winzeler Lab’s Gametocyte Project specializes in the gametocyte stage of the malaria parasites life cycle.

During this stage, the parasite transitions from a liverharbored asexual pest to a red blood cell infecting sexual deviant in a process known as gametocytogenesis. The Gametocyte Project’s current mission: to determine the genes responsible for such a transformation, and to identify drugs that have the potential to block this crucial step in becoming transmissible. The difficulty in answering this question arises in the small percentage of parasites that undergo gametocytogenesis at a given time, and the lack of information and consistent results in inducing the transformation of gametocytes. “At any given moment, only one to three percent of a parasite culture can be found within the gametocyte stage of development at best,” said Alan Du, a second year Molecular Biology

27 Under the Scope • Vol 4

approach to its research.”

Alan has already had a significant impact on the Winzeler Lab. In fact, he was able to grow the highest percentage of gametocytes that the lab has ever cultured.

The New Solution “Finding the genes involved in gametocytogenesis—the process by which asexual parasites become the sexual cells required for human-to-mosquito transmission—will provide invaluable information for researchers working on finding gametocidal drugs that prevent the parasites from becoming transmissible,” said undergraduate researcher Rebecca Stanhope, a member of the Gametocyte Project.

“By blocking the transformation of malaria parasites into gametocytes, the transmission of malaria from human host to mosquito vector is prevented, and thus prevents new cases of infection,” said Rebecca. Gametocidal drugs, or drugs that affect the gametocyte (sexual) stage of malaria parasite’s life cycles, will be fundamental in preventing the spread of malaria and equally important

The parasite responsible for malaria follows a highly complex life-cycle with stages in two different hosts, humans and mosquitos, as well as different stages of development in different cells, red blood cells (RBCs) and liver cells. Gametocytogenesis, the process of becoming a sexually reproducing organism, must occur within the human host’s red blood cells for the transmission of the parasite to a mosquito when feeding. Thus, researchers believe preventing gametocytogenesis will be crucial in preventing human-mosquito transmission and reducing new cases of malarial infection.

in eradicating one of our species’ greatest scourges.

The eradication of malaria would not only mark a biomedical triumph, but a political and economical triumph as well. As a disease of poverty and a leading cause of poverty itself, the eradication of malaria’s influence would reach far beyond the sphere of human health.

WRITTEN BY MAXIMO PRESCOTT, EDGAR VILLARUEL, AND JOHN NICHOLS. Maximo is a Physiology and Neuroscience

major. He will graduate in 2016. Edgar is a Pharmacological Chemistry major and Biology minor. He will graduate in 2016.

John is a Biochemistry and Cell Biology major. He will graduate in 2015.

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Signal Transduction

Research Showcase 2013 Poster Winners

Role of Hexokinase II Dissociation in the Induction of Mitophagy in Cardiac Myocytes Eric Yuxiao Ding Dr. Joan Heller Brown

G protein-coupled Receptor Expression and Function in Pulmonary Artery Smooth Muscle Cells: Novel Targets in Pulmonary Arterial Hypertension Daniel Scott McDonald Dr. Paul A. Insel

Biochemistry and Biophysics

Immunology, Virology and Cancer Biology An Qi Yao

Ecology, Behavior and Evolution

Cell and Developmental Biology

Neurobiology

Climate Change Effects on Soil Microbial Communities: Altered Precipitation and Invasion in a Chaparral System

Does Soil Organic Matter Content Promote Invasive Grasses in Competition With Native Plants in the Anza-Borrego Desert?

Genetic Structure of Leopard Shark Populations Along the Pacific Coast of North America

Using Cell Profiler as an Alternative to Other Methods in Collecting Data Related to the Study of Bacterial Aging

Jun Han Song

Sarah Carmona

Ecology, Behavior and Evolution Nancy Gillcrist

Genetics and Molecular Biology Joanna Coker

Tyler Wishard

Master’s Research Liang Liang Daniel McDonad

Pin-Wen Chen Dr. Paul Price

Studies of Burkholderia pseudomallei’s Type VI Secretion System Protein, VgrG1 Henry Thien-Hoa Quach Dr. Partho Ghosh

Studies on the Mechanisms of Collagen Calcification in Bone Jun Han Song Dr. Paul Price

29 Under the Scope • Vol 4

Amanda Marie Barker Dr. Ron Burton

Are Herbivores Picky Eaters? An Assessment of Functional Diversity of Acanthurids in Maui, Hawaii

Biochemistry and Biophysics Microbial Calcification: A New Method to Combat Microbial Infections at Wound Sites?

Rochelle Aran Dr. Elsa Cleland

Comparison Between the Structural Dynamics of Wild-type and Mutant Fibrinogen Protein Using Amide Hydrogen/ Deuterium Mass Spectrometry Danny Bao Hoang Tran Dr. Virgil Woods Jr. & Dr. Timothy Morris

Structural Dynamic Changes in PrP during Prion Formation as Characterized by Deuterium Exchange Mass Spectrometry Daphne Weihsuan Wang Dr. Virgil Woods

Biochemical Studies of YscO and YscP, two Components of the Type III Secretion System in Yersinia pseudotuberculosis James Yong Wang Dr. Partho Ghosh

Samantha Michelle Clements Dr. Jennifer Smith

Global Assessment of the Status Coral Reef Herbivorous Fishes: Evidence for Fishing Effects Clinton Brook Edwards Dr. Jennifer Smith

Argentine Ant Invasion Reduces Diversity in Mutualist and Parasitoid Guilds Nancy Lee Gillcrest Dr. David Holway

Response of Calcified and Noncalcified Southern California Macroalgae to Increased CO2 and Temperature Susan Laurel Kram Dr. Jennifer Smith

Drinking Dirty Water: Why Do Honey Bees (Apis mellifera) Collect Agricultural Water and Urban Runoff?

Pierre Wai-Kit Lau Dr. James Nieh

Jordan Grey McKinney Dr. Elsa Cleland

Rohan Sushrut Mehta Dr. Lin Chao

The Biodiversity of Arthropods in Organ Pipe (Stenocereus thurberi) Cacti in the Sonoran Desert Dionne Mejia Dr. Therese Markow

Arthropod Species Diversity within Cardon Cacti in the Sonoran Desert Ellen Meryl Reese Dr. Maxi Richmond

Does Size Matter? Prey Size Selectivity of Spotted Sand Bass (Paralabrax maculofasciatus) Amanda Siu Wong Dr. Stuart Sandin

Activating Honey Bee Immunity Against the Widespread Pathogen, Nosema ceranae Adam Jia-Li Yen Dr. James Nieh

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Neurobiology Assessing the Effect of PTEN/Nogo Deletions on Axon Regeneration After Spinal Cord Injury in Mice Omeed Ghassemi Dr. Binhai Zheng

Local Dentate Circuits Support Spatial Working Memory Regardless of Position Along the Longitudinal Hippocampal Axis Ernie Hwaun Dr. Jill Leutgeb

Wnt Inhibition Combined with Pre-conditioning Promotes Plasticity and Functional Recovery Nao Ishiko Dr. Yimin Zou

The Role of Ubiquitin in Neurotransmitter Receptor Trafficking Ruby Kuang Dr. Gentry Patrick

Interneurons Robustly and Consistently Increase Their Firing Rates During the Minutes Preceding Behavioral Seizures in the Chronic Model of Temporal Lobe Epilepsy Liang Liang Dr. Jill Leutgeb

Utilizing Automated Screening Methods to Identify Regeneration Associated Genes Richard F. Lie Dr. Mark H. Tuszynski

Cell and Developmental Biology Muscle-Specific Excision of Polyglutamine-expanded Androgen Receptor Rescues Survival and Neuromuscular Deficits in a Mouse Model of X-linked Spinal and Bulbar Muscular Atrophy Linda Ly Dr. Albert La Spada

Kainate Impairs Pattern Separation and Affects Dentate Gyrus Function in Long Evans Rats Anelah Karina McGinness Dr. Jill Leutgeb

The Role of the Basolateral Amygdala in Mediating Anticipatory Negative Contrast in Binge-like Intake Saba Thaer Naamo Dr. Eric Zorrilla

Reduction of Brain Reward Threshold Elevation During Acute Opioid Withdrawal by Decreasing Noradrenergic Activity in the Central Amygdala Ravi Nuwan Wettasinghe Dr. Gery Schulteis

Control of Neurogenesis by Fragile X Proteins Tyler James Wishard Dr. Hollis Cline

Plant Molecular Biology Expanding the Algal Genetic Engineering Toolkit Kevin Hoang Dr. Stephen Mayfield

Novel Karyopherin Regulation of Mitotic Assembly Events Sarah Lauren Carmona Dr. Douglass J. Forbes

Mouse Genetics to Investigate the Role of Piezo1 in Red Blood Cells Brian Wai Chow Dr. Ardem Patapoutian & Dr. Michael David

The Gene Expression Profile of Abcc5a in Strongylocentrotus purpuratus Embryos Rose Zabel Hill Dr. Amro Hamdoun

Stretch Response of microRNA-148a: Modulation of Inflammatory and Calcification Pathways in Aortic Valve Stenosis Vishal Sanat Patel Dr. Vishal Nigam

The Transmembrane Protein Tmem2 is Essential for Proper Skeletal Muscle Fiber Organization in Zebrafish Jenny Ngoc Tham Phan Dr. Deborah Yelon

Sbf Complex Members Regulate the Toll-signaling Pathway in Drosophila melanogaster

Attenuation of Mitogenic EGFR Signaling by Phosphorylation of GIV, a Non-receptor GEF for Heterotrimeric G-Protein Andrew Thanh-Tam To Dr. Marilyn G. Farquhar

The Role of BMP Signaling in the Development of the Zebrafish Inflow Tract Tina Neda Vajdi Dr. Deborah Yelon

Role of Aminopeptidase O in the Shear Stress-induced Activation of Endothelial Nitric Oxide Synthase in Endothelial Cells Lily Tsenglee Yang Dr. Shu Chien

Protective Effect of Time Restricted Feeding Against NAFLD An Qi Yao Dr. Satchidananda Panda

Telemetry Studies of Caveolin-3 Overexpressing Mice Reveal Characteristics of a Trained Athlete Heart Judith Kumi Yu Dr. Nigel Crawford

Abishek Saluja Dr. Amy Kiger

Systems Biology Characterizing Transcriptional Outputs Mediating Circadian Gene Expression in Arabidopsis thaliana Kellen Yeonsu Na Dr. Mark Estelle

Probiotics Can Normalize the Gut-brain Axis in Immunodeficient Mice Carli Jordan Smith Dr. Kim Barrett & Dr. Melanie Gareau

Conservation of Plant Stress Hormone Responses in the Unicellular Alga, Scenedesmus dimorphus

31 Under the Scope • Vol 4

Fiona Margaret Nohilly Dr. Steven Briggs

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Immunology, Virology and Cancer Biology

Genetics and Molecular Biology Mechanics of Phage201phi2-1 Infection with the Tubulin Protein PhuZ Joanna Katherine Claire Coker Dr. Joe Pogliano

Genomic Organization and Structural Components of Cluster C1 Phage, QBert Alan Yicong Du Dr. Joe Pogliano & Dr. Kit Pogliano

Manipulation of Lipase Activity to Increase Lipid Yields in Thalassiosira pseudonana Jennifer Rachel Hull Dr. William Gerwick

Mechanisms of Thy-1 and its Effects on Signaling Pathways Regulating Myofibroblast Differentiation in Pulmonary Fibrosis Jeeyeon Kim Dr. James Hagood

1) Characterization of the Tetraspanning Junctional Complex (4-JC) Superfamily and 2) Establishing Homology Between Mitochondrial Calcium Uniporters and Prokaryotic Magnesium Transporters Andre Lee Dr. Milton H. Saier

Elucidating Dynamic Interactions of Neuroligin-4-Alpha/ Beta-Neurexin1 Binding via Deuterium Exchange Mass Spectrometry David Eugene Lee Dr. Virgil Woods Jr. & Dr. Palmer Taylor

Drug Screen for Heterochromatin Promoting Drugs in Drosophila melanogaster Andre Christopher Loyola Dr. Willis Li

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Genes Associated with Lysogeny in the“Lytic” Mycobacteriophage Qbert Mekala Kavya Neelakantan Dr. Joe Pogliano & Dr. Kit Pogliano

Investigating the Regulation of GCR1 During Glucose Starvation in the Yeast Saccharomyces cerevisiae.

Sara Lynne Pennebaker Dr. Tracy Johnson

Using Mass Spectrometry to Identify Novel Bacteriophage Nicole Rachel Pollack Dr. Joe Pogliano & Dr. Kit Pogliano

Genetic Studies of a Novel Antisense Transcript Involved in Phycobilisome Degradation in Anabaena sp. Strain PCC 7120 Neil Kamal Raina Dr. James W. Golden

Effects of Beta-lactams on the Proteome of Daptomycin Susceptible and Nonsusceptible Methicillin-resistant Staphylococcus aureus (MRSA) Chiara Jeun-Ning Elena Ricci-Tam Dr. Joe Pogliano

Role for AMPK-activators In Treatment Of Cryopyrinassociated Periodic Syndromes (CAPS)

Role of Splicing Factor SC35 in the Whole Blood System and in the Development of MDS.

Akemi L. Brown Dr. Harold Hoffman

Leo I-Chuan Lin Dr. Dong-Er Zhang

Characterization of the Interaction Between Caspase-8 and p85

Effects of Streptolysin O in Drosophila Development and Roles of HIF1 in Toxin-mediated Apoptosis

Lauren Elizabeth Chen Dr. Dwayne G. Stupack

Severity of Murine Arthritis Modulated by Neutrophil Cell Death via Interferon and IKKe Pathways Christopher Sai-Hau Chung Dr. Maripat Corr

Paracrine Wnt Signaling Both Promotes and Inhibits Human Breast Tumor Growth Payal P. Desai Dr. Geoffrey Wahl

Vpu Activity of Transmitted/Founder and Chronic Clade B HIV-1 Moein Jafari Dr. John Guatelli

Aaron Louie Dr. Victor Nizet

The Role of Interleukin-11 in Pancreatic Cancer Progression Jaclyn Kuniko Miyamoto Dr. Andrew M. Lowy

Drug Strategies to Enhance Autophagic Death in Ovarian Cancers Parthiv Vipul Sheth Dr. Dwayne Stupack

Whole Blood microRNA Profiles in Adenovirus-infected Children Christine Trinh Dr. Jane C. Burns

Identifying Novel Transport Proteins Promoting E. coli Pathogenesis

Regulation of microRNAs by mTOR in Head And Neck Squamous Cell Carcinoma Selena Zhao Kuo Dr. Jens Lykke-Andersen

Zhi-Fang Tsun Dr. Ye Zheng

Identification of 3’UTR Elements that Inhibit Nonsensemediated Decay

Characterization of Cell Cycle Progression Using a Novel Bi-cistronic Lentiviral FUCCI Reporter

Gut Lactobacillales are Associated with Higher CD4 and Less Microbial Translocation during HIV Infection

Florence Lambert-Fliszar Dr. Catriona Jamieson

Susanna R. Var Dr. David M. Smith

Genes Involved in the Lytic Pathway of Mycobacteriophage Qbert

Hh Signaling Regulates KIT Expression in Gastrointestinal Stromal Tumors

Role of Epithelial microRNAs During Rotavirus Infection in Humans

Viral Transduction of Human Cancer Cell Lines with an Optimized Triple Modality Reporter for Quantifiable Tumor Imaging and Therapy Evaluation In Vivo

Characterizing the Role of NETs in the K/BxN Mouse Model of Rheumatoid Arthritis

Fengyi Tang Dr. Milton H. Saier

Kalodiah Gorges Toma Dr. Jens Lykke-Andersen

Victoria Marie Winslow Dr. Joseph Pogliano

Using Next-Generation Mapping Methods to Identify Genes that Mediate Responses to Water Limitation in Plants Eric Jie Yang Dr. Julian Schroeder

Tracy Ellen Lee Dr. Jason K. Sicklick

Rachel Ashley Levin Dr. Roger Tsien & Dr. Quyen Nguyen

In Vitro Model for Fat-resident Regulatory T cells

Kim Ngoc Vu Dr. Martin Kagnoff

Joshua Young Cynming Yang Dr. Maripat Corr

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